Varicella Zoster Virus and Stroke

Introduction

Varicella zoster virus (VZV) is a ubiquitous, neurotropic alphaherpesvirus. Primary infection usually causes varicella (chickenpox), after which virus becomes latent in cranial nerve, dorsal root, and autonomic ganglionic neurons, including enteric ganglionic neurons and adrenal cells.

With a decline in VZV-specific cell-mediated immunity in elderly and immunocompromised individuals, virus reactivates from one or more ganglia and typically travels along nerve fibers peripherally to produce herpes zoster (shingles) in the corresponding dermatome(s), which can be complicated by postherpetic neuralgia. VZV can also travel centrally to produce ocular and neurological disease with or without rash, including stroke due to productive virus infection of cerebral arteries (VZV vasculopathy). Early cases of VZV vasculopathy were described as a contralateral hemiparesis associated with herpes zoster ophthalmicus or as a postvaricella angiopathy, typically presenting as a hemiparesis during or shortly after varicella. Today, the clinical spectrum of VZV vasculopathy has expanded to include transient ischemic attacks (TIAs), hemorrhagic or ischemic stroke, aneurysm, and sinus thrombosis, as well as giant cell arteritis (GCA)—all occurring with or without rash. Since VZV is latent in >90% of the world population and will reactivate in 50% of individuals by 85 years of age, and since our aging population continues to increase, VZV vasculopathy will continue to play a significant role in stroke. Herein, the epidemiology of stroke associated with zoster, the clinical features and management of VZV vasculopathy and its pathogenesis will be reviewed.